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Fenster schliessen

Biological theories of panic; Serotonergic theory

• Dysfunctional neurotransmission at the serotonin receptors (5HT1A) may result in

anxiety or avoidant behavior (Deakin 1996)

• Activation of HPA Axis in panic disorder, may contribute to disruption of

hippocampal 5HT1A

neurotransmission (Lesch and Lerer 1991)

• Aberrant noradrenergic- serotonergic function (Boyer 1995)

• Serotonin depletion resulted in increased minute ventilation in panic disorder


unaltered ventilatory function in controls (Kent et al., 1996)

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Biological theories of Panic; GABAergic Theory

• GABA = inhibitory neurotransmitter

• Benzodiazepines increase function of GABA

• global decrease in benzodiazepine binding

• with a peak decrease in orbitofrontal cortex, and insula, hippocampus in panic

disorder patients compared to healthy controls (Malzia et al., 1998)

• Injection of sodium lactate (panicogen) led to panic-like response in

GABA-blocked rats only (Shekhar 2006)

• Interaction GABA-glutamate interrupted in panic disorder

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Role of Panicogens in Panic Disorders

= substances that can induce panic attacks

substances that influence HPA Axis

Yohimbine (noradrenaline increase)

coffein: adenosinergic (inhibitory) receptor antagonist

Substances that influence lactate metabolism

sodium lactate, sodium bicarbonate, carbon dioxide

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Role of Genetics in the Pathogenesis of Panic Disorder

• Twin studies have attributed 30-40% of the variance for the liability to develop

panic disorder to genetic factors (Kendler et al., 2001; Scherrer et al. 2000)

• highly significant association between panic disorder in probands

and first degree relatives (Hettema et al. 2001)

• cholecystokinin, adenosine 2A, MAO A, and COMT genes.

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Psychological Theories of Panic Disorder

Dynamic Model:

panic attack = expression of an intense unconscious conflict (Bush et al. 1999)

core conflict of depencency and inadequacy (Shear et al. 1993)

Contemporary dynamic models: integration of biological and developmental stressors

(Milrod et al. 2004)

Cognitive Behavioral Models

Anxiety Sensitivity

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Theoretical perspective: cognitive factors

Anxiety sensitivity (Reiss and Mc Nally (1985)

• Core fear toward anxiety and its associated somatic symptoms

• Measured by anxiety sensitivity index

(Reiss et al. 1986)

• Significant predictor of the onset of panic in different patient populations

(e.g Ehlers 1995, Hayward et al. 2000; Maller and Reiss 1992)

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Hyperventilation & Respiratory Theories

• Ley (1985): hyperventilation theory : hyperventilation causes panic attacks

• Klein (1993): false suffocation alarm model: hyperventilation avoid panic


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Suffocation false alarm theory

Person is hypersensitive to carbon dioxide levels ⇒ Minor drops in Oxygen result in false alarm "person is suffocating" ⇒ Panic Attack

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Pharmacological treatment for panic disorder

First line treatments

• SSRI (Selective Serotonin Reuptake Inhibitors)

effective in many controlled studies ( e.g. Wade et al. 1997; Michelson et al 1998, 2000)

anxiolytic effect latency of 2-4 weeks

• Serotonin Norepinephrine Reuptake Inhibitors

effective in double blind placebo controlled studies (Bradwejn et al. 2005; Pollack et al. 1996)

Second line treatments

• Tricyclic antidepressants

frequency of adverse events is higher than for SSRI (Amore et al. 1999)

Third line treatments

• Benzodiazepines

anxiolytic effects immediately after oral intake, risk of dependency (Bradwejn 1993)

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Psychological treatment for panic disorder

Cognitive behavioral therapy

“Panic control treatment”

(PCT, Craske et al., 2000, Hofmann & Spiegel, 1999)


• Education about anxiety and panic development

• Cognitive restructuration: identification and correction of thoughts /

false cognitions about anxiety and its consequences

• Training (reduction arousal, hyperventilation)

• Exposition, controlled hyperventilation

11-12 sessions, 3-4 months

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Psychological treatment for panic disorder


Classical CBT Methods

• Hyperventilation

• Triggering bodily symptoms

• Deep breathing

• External focus

• mindfulness

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Learning safety in panic

Interoceptive exposure

Feared sensations become safe sensations:

• in the office with the therapist

• at home

• independent of the treatment context

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Panic Cycle

Uh oh!

What if:

• This gets worse?

• I lose control?

• This is a stroke?

I have to control


Relative Comfort

• Notice the sensation

• Do nothing to control it.

• Relax WITH

the sensation

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Exposure procedures

Head rolling – 30 seconds - dizziness, disorientation

Hyperventilation – 1 minute - produces dizziness

lightheadedness, numbness, tingling, hot flushes, visual


Stair running – a few flights – produces breathlessness, a

pounding heart, heavy legs, trembling

Full body tension – 1 minute – produces trembling, heavy

muscles, numbness

Chair spinning – several times around – produces strong

dizziness, disorientation

Mirror (or hand) staring – 1 minute – produces derealization

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Psychological treatment for panic disorder

Cognitive behavioral therapy

• Efficacy between 87% and 75%

• Greater efficacy than relaxation therapy or control groups

• Greater efficacy than certain medicaments (e.g. alprazolam) and

similar to imipramine

• Long-term treatment with PCT is more effective than pharmacological


• Evidence of superiority from combined approach towards single treatment

not conclusive

• New developments: combination with self-help modules, therapy via

internet, electronic auto-observation

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Anxiety is a multidimensional experience (systems)

  • Emotional symptoms
  • Cognitive symptoms
  • Physiological symptoms
  • Behavioral symptoms


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Classical Conditioning

- Watson & Raynor (1920): “little Albert”

- extension by Mowrer (1960) conditioning is mediated by motivations such as

desire to reduce fear, accounts for avoidance behavior

Shortcomings (Rachman et al. 1991 for review)

- all stimuli can become feared stimuli (the equipotenitality premise)

- many people experience aversive conditioning but do not develop a phobia

- traumatic etiology is not reported by all phobic individuals

- limited success of studies that have endeavored to condition stable fears in human in an experimental setting

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Vicarious conditioning

  • learning by observing reactions of others Bandura & Rosenthal, 1966 Bobo Doll experiment.
  • Verbal information (e.g. media, Rachmann, 1991)
  • witnessing someone else have a fearful reaction or upsetting social experience
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Seligman (1971) phobic stimuli are biologically threatening humans are biologically prepared to develop fears of stimuli that threaten personal safety

four features of prepared phobias:

- acquired through one-trial conditioning

- non-cognitive

- phobic object involves threat to humankind, result of natural selection

- not easily extinguished

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Multiple pathways

Rachman (1991) several alternative pathways

(direct conditioning, model learning, verbal acquisition)



- Bandura (1966): participants had to watch person receiving electro-shock,

resulted in increase in physiological response by just viewing apparatus

- Cook and Mineka (1989): monkeys watched videotapes of monkeys behaving

fearfully to either fear relevant (snakes, crocodiles) fear irrelevant stimuli (flowers,

rabbits, development of fear of the fear-relevant stimuli, replicated by several studies

- acquisition via verbal information in the epidemics of koro in Singapore and Thailand.

The epidemics were thought to have been caused by verbal transmission via media

(Rachman 1991)

- increases in skin conductance in response to target stimulus after information that stimulus

would be followed by a shock (Cook & Harris 1937)

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Non-associative theory

Phobias may be acquired without previous direct or indirect

associative learning (Menzies and Clarke 1995)


- (Menzies & Clarke, 1993): Interviewing parents of children with water phobia

only 1 percent out of 50 could recall a classical conditioning episode, and 58%

of the parents reported that the fear had always been present

- retrospective reports from phobic patients lack of direct conditioning in height

phobia, spider phobia (Jones and Menzies, 1995)

- separation anxiety in human infants and mammals has been found to be unrelated

to past aversive experiences of separatin (Bowlby 1973)

conclusion: learning experiences (verbal, direct, associative) are not necessary for

the development of phobias, normal childhood concerns become phobias in some

individuals by two means:

- learning to successfully avoid an object (parents used avoidant coping styles, verbal


- dishabituation of childhood fears during stressful periods (Menzies & Clarke, 1993)

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Biological factors

- genetic component: higher risk among first-degree relatives (Fyer et al. 1990)

- mixed results regarding genetic vs. environmental contribution (Bolton et al. 2006)

- genetic contribution varies to subtype – more specific genetic contribution for

blood phobia (Fyer et al. 1990)

- neuropathophysiology remains poorly understood (Fyer et al. 1998)

mixed results about amygdala hyperactivation as in other anxiety disorders

(Gossens et al. 2007)

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Cognitive factors

cognitions play a role in maintainance (Rachmann 1991)

- cognitions increase arousal and likelihood of escape or avoidance (Last 1987)

empirical support:

- exposition to feared situation lead to triggering of negative self-statements, which

heighten physiological activity (Last and Blanchard 1982)

- most patients report at least one unrealistic belief about the harm that could befall

them when confronted with object or situation (Thorbe and Salkovskis 1995)

- attentional bias toward phobia related threats (Burgees 1982, Mogg et al.2004)

- Stroop paradigm: phobic individuals are slower to name the color of threat related

words (Constantine et al, 2001)

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Exposure therapy

More effective than insight-oriented group or individual psychotherapy (Gelder et al. 1967)

Four approaches:


In vivo exposure


Systematic desensitization (Wolpe 1958)

• Gradual

• Prolongued exposure -> psychoeducation

• Therapist needs to be comfortable with phobic object

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Treatment options

• Eye movement desensitization and Reprocessing

• Hypnotherapy: several studies reported success of hypnosis in phobia treatment

(Bird 1997, Ginsberg 1993, Morgan 2001)

-> group studies no comparison group (Peretz et al. 1996), many dropouts

(Hamarstrand et al. 1995)

• Psychopharmacology:

not treatment of choice for specific phobia (Roy-Byrne and Cowley, 2007)

studies using benzodiazepines showed no evidence of

long-term reductions in anxiety or avoidance (Campos et al. 1984)

based on preliminary studies

• Blood-Injection-Injury phobia: treatment complicated by fainting

applied tension-> tensing various muscle group during exposure

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Epidemiology; Social Anxiety

• One of the most common psychological disorders

• Lifetime prevalence rates for SAD based on large community samples range

from 3 to 13% (Kessler et al., 2005)

• Tends to begin in adolescence (mid / late teens) but also earlier possible

• Mean onset 15.7 years (Brown et al. 2001) -> lower compared to other AD

• Onset later in adulthood are rare and may be secondary to another mental disorder

(social withdrawal MDD, avoidance of eating in public)

• SAD slightly more common in women than men (Fehm et al., 2005)

• Gender differences in presentation of SAD (Turk et al. 1998)

women: talking to people of authority, performing in front of audience, working while

being observed, entering a room where others are already seated, being center

of attention, expressing disagreement, throwing a party

men: returning goods to a store, urinating in a public bathroom

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The cognitive model of Clark and Wells (1995)

• People with SAD are invested in making a positive impression on others, but

are insecure about ability to do so

• They hold negative beliefs about themselves and their ability to perform in social


• When in social situations people with SAD focus on themselves and see

themselves as if they’re watching themselves on television

• Focusing on themselves doesn’t allow people with SAD to fully participate

in the social situation

• People with SAD either avoid situations of use safety behaviors in feared


• Safety behaviors and avoidance do not allow the person to learn that fears

may not actually come true

• Negative thinking about social situations occurs before, during and after

exposure to the situation

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The cognitive behavioral model of Rapee and Heimberg (1997)

• Source of perceived threat for people with SAD is the belief that others hold

unreasonable high expectations of them, “reaction of an audience”

• audience reaction ->mental representation

• Mental representation is influenced by self-image from memory, pictures, physical

symptoms and social feedback

• Mental representation often distorted: people with SAD rate their performance as

poor, even if not objectively true

• Feedback often distorted or twisted to be consistent with fears

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Negative learning experiences in SAD

• People with SAD report a history of childhood teasing more often than people without

SAD (Mc Cabe et al. 2003)

• Severe bullying during childhood related to higher frequency of SAD

(Gladstone et al., 2006)

• Lacking social experiences (socially anxious individuals often raised by socially

isolated parents (Bögels et al. 2001)

• Observational studies: parents of anxious children support more likely desire of

child to be avoidant (Dadds et al. 1996)

• However, negative learning cannot fully explain how SAD develops

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Psychological treatment options for SAD

• Studies comparing CBT to other psychotherapies for SAD, CBT superior

(Rodebaugh et al.2004)

• The most frequently studied, evidence based psychological strategies for SAD


- cognitive strategies (identifying anxiety provoking thoughts, replace such thoughts with

more realistic thoughts and predictions, behavioral experiments to test validity of anxious


- exposure-based-strategies

- social skills training (improve social and communication skills, eye contact, body language,

making small talk..)

• Mixed results: combination of exposure plus cognitive therapy works better than

exposure alone. Other studies found exposure alone just as effective (Rodebaugh et al.,2004)

• In addition some studies suggest that applied relaxation (PMR combined with

exposure) is also useful (Rodebaugh et al. 2004)

• Social skills training has been shown to improve effectiveness of CBT, other studies

found no difference between CBT with or without social training (Rodebaugh et al. 2004)